ABSTRACT
Objective Bile acids (BA) facilitate cholesterol hepatic fibrosis. Although hepatic stellate cell (HSC) is one of the moot important cells during liver fibrogenesis, the effect of bile acids on HSC is rarely mentioned. Therefore,bile acids facilitate liver fibrosis through regulating activated HSC should be tested. Methods The amount of BrdU incor-poration was determined to assess the proliferation of HSC treated by bile acid. Wound-healing assay was used to determine the cellular motility. Meanwhile, the phoophorylation of p38 and JNK in HSC was detected by Western blotting. Results50 μmol/L GCDCA enhanced the HSC proliferation significantly (152.0% ± 7.1%, P < 0.05); 50 μmol/L GCDCA also induced phoophorylation of p38 and JNK (450.0% ± 12.2% of control in p38 (P < 0.01 ), 210.0% ± 15.2 % of control in JNK (P<0.05)). 50 μmol/L GCDCA aided wound healing (remaining wound area is 75.4% + 5.8% of original area, P<0.05), but this effect was inhibited by JNK (SP600125) or p38 (SB294002) inhibitor, respectively. Conclusions Bile acids enhance HSC proliferation and facilitate cellular motility through inducing phosphorylation of p38 and JNK, indicating bile acid aid liver fibrosis through regulation of p38 and JNK signaling.